Plus Kits ELISA pour CHL1 partenaires d'interaction

Expression level of miR-21-5p increased in both colon adenocarcinoma (COAD) tissues and cells. The result of in vivo experiments showed that down-regulation of miR-21-5p decreased the volume and weight of tumor, while knockdown of CHLI stimulated tumor growth. The overexpression of miR-21-5p can promote propagation and invasiveness of (COAD) cells through inhibiting the expression of CHL1.

CHL1 was found to have greater than 15-fold higher expression in fragments per kilobase million in HCC compared with benign Hurthle cell tumors. This was confirmed by qRT-PCR. Moreover, the immunoreactivity score of the CHL1 protein was significantly higher in HCC compared with benign Hurthle cell nodules.

Results indicate that close homolog of L1 protein (CHL1) is downregulated by hypermethylation and that this epigenetic alteration is an independent prognostic factor in breast cancer (BC).

here we identify a number of novel roles for CHL1 in establishment of the midbrain dopamine pathways, functions that are reinforced by evidence in other neuronal networks, yet roles that are also unique to this discrete population of neurons. Supported by spatial and temporal expression within the VM, and validated in CHL1 deficient mice.

The correlation between the tumor size and the amount of CHL1 secretion could be examined in this study, and showed a significant positive correlation in a tumor size-dependent manner.

investigated temporal discounting in CHL1-deficient (KO) mice and their wild-type littermates. Although no discounting differences were found under baseline conditions, CHL1-KO mice showed increased impulsive choice following chronic unpredictable stress (fewer % larger-later choices, and reduced area under the discounting curve). Impulsive choice alterations were reversed by the 5-HT2C agonist Ro 60-0175.

The results of the present study indicate that CHL1 triggers PTCH1-, SMO-, RhoA- and ROCK-dependent signal transduction pathways to promote neuronal survival after cessation of the major morphogenetic events during mouse cerebellar development.

These results provide strong support for a 'two-hit' (genes x environment) effect on latent inhibition in CHL1-deficient mice, and identify CHL1-deficient mice as a model of schizophrenia-like learning and attention impairments.

Findings indicate that disrupted-in-schizophrenia 1 (DISC1) and close homolog of L1 may engage in physical and functional interaction in neural development, supporting the notion that DISC1 regulates neurite outgrowth with a receptor belonging to the neural cell adhesion molecules.

CHL1 is a novel intrinsic factor that is involved in carotid body function and in the ventilatory response to acute hypoxia.

CHL1 endocytosis are required for CHL1-dependent neurite outgrowth.

CHL1 might play an important role in hypoxia damage regulation.

BACE1(-/-) axon guidance defects are likely the result of abrogated BACE1 processing of CHL1 and BACE1 deficiency produces a CHL1 loss-of-function phenotype

L1 and CHL1 are cleaved by BACE1 under physiological conditions

This study provided evidence that the CHL1 affect the repair of the blood-spinal cord barrier repair in soinal cord injury.

Results describe the negative modulation of the proliferation and neuronal differentiation of neural progenitor cells by CHL1/ERK1/2 MAPK signaling.

The results of this study implicated a novel mechanism in which L1 and CHL1 interact with individual EphA receptors and cooperate to guide subpopulations of thalamic axons to distinct neocortical areas essential for thalamocortical connectivity.

data show that the permanent absence of CHL1 results in misguided axonal projections and aberrant axonal connectivity and alters the exploratory behavior in novel environments, suggesting deficits in information processing in CHL1-deficient mice.

CHL1 profil antigène

Antigen Summary

The protein encoded by this gene is a member of the L1 gene family of neural cell adhesion molecules. It is a neural recognition molecule that may be involved in signal transduction pathways. The deletion of one copy of this gene may be responsible for mental defects in patients with 3p- syndrome. This protein may also play a role in the growth of certain cancers. Alternate splicing results in both coding and non-coding variants.